8/14/2019 Keep the Pressure Up and Don't Spare Vasoconstrictor Editorial

1/3

8/14/2019 Keep the Pressure Up and Don't Spare Vasoconstrictor Editorial

2/3

responsive to vasoconstrictors compared with those from

non-pregnant ewes. Giving large doses of alpha-agonists

that constrict peripheral arteries and restore normal maternal

arterial pressure may preferentially shunt blood to the

uterine arteries, which may be relatively spared from the

vasoconstrictive effect.

We must also consider the possibility that signicant

placental vasoconstriction does occur with phenylephrine,

but may not be important with regard to fetal wellbeing. Ofparticular interest in Kee and colleagues' article in the

current issue1 is the trend for an increase in umbilical artery

PO2 to occur in conjunction with higher maternal arterial

pressures (although this did not quite reach statistical

signicance P=0.058). This nding is consistent with my

observations during ex utero intrapartum therapy pro-

cedures and fetal surgery. In these cases, the fetus is at

least partially extracted from the uterus but not separated

from the placenta. The fetus continues to be supported by

the placenta while a procedure is performed. In all instances,

a pulse oximeter probe was placed on the fetus. In these

cases (performed under general anaesthesia with high-dose

potent inhalational anaesthetics given to provide uterinerelaxation), I have observed an increase in fetal oxygen

saturation of 1020% when maternal arterial pressure was

increased after administration of a vasopressor (ephedrine

or phenylephrine) to the mother. Why should maintaining a

higher arterial pressure increase oxygen delivery across the

placenta? It may be simply that a higher perfusion pressure

delivers more blood to the placenta and that this favourable

effect far outweighs any variations in placental vascular

diameter resulting from the doses of pressors used in recent

clinical studies.

Although the current study1 demonstrates that maintain-

ing a higher arterial pressure increases the umbilical artery

pH, is the difference of 0.02 clinically signicant? Perhapsnot in the healthy fetus. However, there will be cases in

which compromised fetuses may benet signicantly by

having maternal arterial pressure maintained and fetal

oxygen delivery optimized. For example, Datta and

Brown9 showed that umbilical artery pH was only slightly

decreased after Caesarean delivery in healthy mothers who

experienced transient hypotension secondary to their spinal

anaesthetic. However, in infants of diabetic mothers who

developed similar degrees of hypotension, the umbilical

artery pH decreased to a clinically signicant level. Since

we do not always know the adequacy of placental reserve, it

makes sense to always maintain the arterial pressure near to

normal values, given the data presented in Kee and

colleagues' paper.1

While it may appear logical to assume that what

constitutes good therapy for normal mothers and fetuses

constitutes good therapy for the compromised maternal

fetal unit, this may not always be the case. In reality, we do

not really know how ndings in normal subjects transfer to

unhealthy mothers or fetuses. For example, what is the

optimal maternal arterial pressure for a pre-eclamptic

patient? In a recent study, Dyer and colleagues10 found

that among patients with severe pre-eclampsia, the outcome

for the baby was better if the mother had a general

anaesthetic rather than a spinal anaesthetic. The spinal

anaesthetic group received more ephedrine and presumably

suffered from a greater incidence of hypotension compared

with the general anaesthetic group. Would the outcome have

favoured spinal anaesthesia had that group's arterial pres-

sure been managed more aggressively with phenylephrine?The paper by Kee and colleagues1 does not answer this

question, but important studies usually create more ques-

tions than they answer. Numerous studies have now

demonstrated the superiority of phenylephrine for manage-

ment of spinal hypotension in healthy mothers and babies.

We now need more studies on the effects of hypotension and

vasoconstrictors in situations of maternal or fetal comprom-

ise.

Although there is much more to learn about hypotension

and spinal anaesthesia for Caesarean delivery, we already

have a wealth of information to help guide therapy. How

should we prevent and treat the hypotension associated with

spinal anaesthesia? The following are my recommenda-tions:

Leg wrapping. A recent meta-analysis11 showed that

wrapping the legs with elastic bandages or the use of

thromboembolic stockings prevents hypotension.

Colloid preload. The same meta-analysis11 found that

colloid preloads prevented hypotension and the individual

studies found improvements in outcome measures such as

Apgar scores, ephedrine use, lower maternal heart rate, less

nausea and less severe hypotension.1214 Crystalloid pre-

loads are largely ineffective.

Eliminate or drastically limit the use of ephedrine. Every

study that has compared ephedrine and phenylephrine has

found more acidosis in the fetus when the mother was givenephedrine.4 Although it makes theoretical sense to restore

both beta- and alpha-adrenergic tone after the induction of a

high sympathectomy from spinal anaesthesia, limit the use

of ephedrine. For anaesthetists who are concerned with the

possible bradycardia associated with a high spinal or the

reex bradycardia associated with the use of vasoconstrict-

ing drugs such as phenylephrine, the use of a mixture of

ephedrine and phenylephrine will keep the heart rate up and

the dose of ephedrine low enough not to be detrimental to

the fetus.7

Treat the hypotension aggressively. To reiterate what I said

earlier, the use of ephedrine leads to acidosis in the fetus.

The aggressive use of phenylephrine and other pure alpha-

vasoconstrictors is apparently the best practice. At least, that

is what the data provided by Kee and colleagues suggest.

The data in the literature support the above practices.

Now what are needed are studies that evaluate how these

changes in management affect outcomes. With the new

management strategies, will the umbilical artery pH in

babies delivered to mothers having spinal anaesthesia be as

good as the values of the mothers having epidural or general

Editorial I

460

8/14/2019 Keep the Pressure Up and Don't Spare Vasoconstrictor Editorial

3/3

anaesthesia? Can we decrease adverse neurological out-

comes? Will there be fewer neonatal intubations or admis-

sions to the neonatal intensive care units? Are these the

optimal strategies for the compromised maternalfetal unit?

Hopefully, Kee and colleagues will continue their excellent

work and help us answer some of these questions.

E. T. Riley

Associate ProfessorDepartment of Anesthesia

Stanford University School of Medicine

Stanford

California 94305

USA

E-mail: edriley@Leland.stanford.edu

References1 Kee WD, Khaw KS, Ng FF. Comparison of phenylephrine

infusion regimens for maintaining maternal blood pressure

during spinal anaesthesia for Caesarean section. Br J Anaesth

2004; 92: 46974

2 Ralston DH, Shnider SM, DeLorimier AA. Effects of equipotent

ephedrine, metaraminol, mephentermine, and methoxamine on

uterine blood ow in the pregnant ewe. Anesthesiology 1974; 40:

35470

3 McGrath JM, Chestnut DH, Vincent RD, et al. Ephedrine remains

the vasopressor of choice for treatment of hypotension during

ritodrine infusion and epidural anesthesia. Anesthesiology 1994;

80: 107381; discussion 28A

4 Ngan Kee WD, Lee A. Multivariate analysis of factors associated

with umbilical arterial pH and standard base excess after

Caesarean section under spinal anaesthesia. Anaesthesia 2003;

58: 12530

5 Cooper DW, Carpenter M, Mowbray P, Desira WR, Ryall DM,

Kokri MS. Fetal and maternal effects of phenylephrine and

ephedrine during spinal anesthesia for cesarean delivery.

Anesthesiology 2002; 97: 158290

6 Wright RG, Shnider SM, Levinson G, Rolbin SH, Parer JT. The

effect of maternal administration of ephedrine on fetal heart rate

and variability. Obstet Gynecol 1981; 57: 7348

7 Mercier FJ, Riley ET, Frederickson WL, et al. Phenylephrine

added to prophylactic ephedrine infusion during spinal anesthesia

for elective cesarean section. Anesthesiology 2001; 95: 66874

8 Tong C, Eisenach JC. The vascular mechanism of ephedrine's

benecial effect on uterine perfusion during pregnancy.Anesthesiology 1992; 76: 7928

9 Datta S, Brown WU, Jr. Acidbase status in diabetic mothers and

their infants following general or spinal anesthesia for cesarean

section. Anesthesiology 1977; 47: 2726

10 Dyer RA, Els I, Farbas J, Torr GJ, Schoeman LK, James MF.

Prospective, randomized trial comparing general with spinal

anesthesia for cesarean delivery in preeclamptic patients with a

nonreassuring fetal heart trace. Anesthesiology 2003; 99: 5619;

discussion 56A

11 Morgan PJ, Halpern SH, Tarshis J. The effects of an increase of

central blood volume before spinal anesthesia for cesarean

delivery: a qualitative systematic review. Anesth Analg 2001; 92:

9971005

12 Mathru M, Rao TL, Kartha RK, Shanmugham M, Jacobs HK.

Intravenous albumin administration for prevention of spinal

hypotension during cesarean section. Anesth Analg 1980; 59:

6558

13 Riley ET, Cohen SE, Rubenstein AJ, Flanagan B. Prevention of

hypotension after spinal anesthesia for cesarean section: six

percent hetastarch versus lactated Ringer's solution. Anesth Analg

1995; 81: 83842

14 Siddik SM, Aouad MT, Kai GE, Sfeir MM, Baraka AS.

Hydroxyethylstarch 10% is superior to Ringer's solution for

preloading before spinal anesthesia for Cesarean section. Can J

Anaesth 2000; 47: 61621

DOI: 10.1093/bja/aeh084

Editorial II

The Board of Management and Trustees of the British Journal of Anaesthesia 2004